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Tissue gas tensions and tissue metabolites for detection of organ hypoperfusion and ischemia

Authors

  • L. WÆLGAARD,

    1. The Acute Clinic, Department of Anesthesiology and Critical Care Medicine, Oslo University Hospital, Oslo, Norway
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  • B. M. DAHL,

    1. The Intervention Centre, Oslo University Hospital, Oslo, Norway
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  • G. KVARSTEIN,

    1. The Acute Clinic, Department of Anesthesiology and Critical Care Medicine, Oslo University Hospital, Oslo, Norway
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  • T. I. TØNNESSEN

    Corresponding author
    1. The Intervention Centre, Oslo University Hospital, Oslo, Norway
    2. Institute for Clinical Medicine, University of Oslo, Oslo, Norway
    • The Acute Clinic, Department of Anesthesiology and Critical Care Medicine, Oslo University Hospital, Oslo, Norway
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  • Funding received: The Norwegian Research Council, The Research Council of Rikshospitalet, and Småforskmidler from the Faculty Division, Rikshospitalet.

Address:

Tor Inge Tønnessen

Oslo University Hospital – Rikshospitalet

Box 4950 Nydalen

N-0424 Oslo

Norway

e-mail: t.i.tonnessen@medisin.uio.no

Abstract

Background

The aim of this study was to evaluate how tissue gas tensions and tissue metabolites measured in situ can detect hypoperfusion and differentiate between aerobic and anaerobic conditions during hemorrhagic shock. We hypothesized that tissue PCO2 (PtCO2) would detect hypoperfusion also under aerobic conditions and detect anaerobic metabolism concomitantly with or earlier than other markers.

Methods

Prospective experimental animal study with eight anesthetized pigs subjected to a continuous blood loss ∼ 8% of total blood volume per hour until death. We measured cardiac index, organ blood flows, and tissue levels of PO2, PCO2, glucose, pyruvate, lactate, and glycerol in intestine, liver, kidney, and skeletal muscle.

Results

With reduction in blood flow to the organs under aerobic conditions, PtCO2 increased ∼ 1–4 kPa from baseline. With the onset of tissue hypoxia there was a pronounced increase of PtCO2, lactate, lactate-pyruvate (LP) ratio, and glycerol. Tissue pH and bicarbonate decreased significantly, indicating that metabolic acid was buffered by bicarbonate to generate CO2.

Conclusion

Moderate tissue hypoperfusion under aerobic conditions is associated with increased PtCO2, in contrast to metabolic parameters of ischemia (lactate, LP ratio, and glycerol) which remain low. From the onset of ischemia there is a much more rapid and pronounced increase in PtCO2, lactate, and LP ratio. PtCO2 can be used as a marker of hypoperfusion under both aerobic and anaerobic conditions; it gives an earlier warning of hypoperfusion than metabolic markers and increases concomitantly with or earlier than other markers at the onset of tissue anaerobiosis.

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